Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma glucagon and growth hormone concentrations were measured fasting and after oral glucose in 19 patients with portal vein block with extensive portal-systemic shunting but minimal liver cell damage, 11 cirrhotic patients and 12 matched control subjects. Portal vein block patients and controls had similar fasting glucose and glucagon levels (glucose 3.8 +/- 0.1 mmol/l VS control 3.4 +/- 0.1 mmol/l (mean +/- SEM); glucagon 57.5 +/- 9.1 pg/ml VS control 51.3 +/- 7.8 pg/ml). Cirrhotic patients were hyperglycaemic (cirrhosis 4.3 +/- 0.2 mmol/l VS control 3.4 +/- 0.1 mmol/l, p < 0.01) with significantly elevated glucagon levels (167.3 +/- 61.1 pg/ml VS control 51.3 +/- 7.8 pg/ml, p < 0.05), which suppressed towards control values after oral glucose. There was no correlation between fasting plasma glucagon levels and the degree of portal-systemic shunting in cirrhotic patients. There was a strong correlation between fasting plasma glucagon concentrations and aspartate transaminase levels (r = 0.68; p < 0.01) in cirrhotic and portal vein block patients. Significant elevations of growth hormone were seen only in cirrhotic patients. It is concluded that hyperglucagonaemia is a feature of hepatocellular damage rather than portal-systemic shunting but the relationship between elevated glucagon and growth hormone concentrations and carbohydrate intolerance in cirrhosis remains unclear.
 ...
PMID:Hyperglucagonaemia in cirrhosis. Relationship to hepatocellular damage. 741 64

Nine patients with compensated alcoholic and nonalcoholic cirrhosis of the liver and 11 patients with peptic ulcer received 200 mg of cimetidine orally and intravenously. No differences were observed in cimetidine clearance between the group with peptic ulcer (556 +/- 44 ml/min, mean +/- SEM) and the group with cirrhosis (606 +/- 64 ml/min). The bioavailability of cimetidine was unchanged (84 +/- 4% and 97 +/- 7%). In the patients with cirrhosis, cimetidine clearance did not correlate with galactose elimination capacity or antipyrine clearance. Cimetidine clearance was related to creatinine clearance only when both groups were considered. A reduction of cimetidine dose in patients with compensated cirrhosis appears unwarranted.
 ...
PMID:Cimetidine clearance and bioavailability in hepatic cirrhosis. 746 Apr 83

Numerous abnormalities of plasmatic coagulation and platelet function may contribute to the bleeding in liver cirrhosis with a defective platelet-von Willebrand factor interaction being a potential mechanism. To analyze GPIb and von Willebrand factor in cirrhosis, we quantified the number of GPIb molecules on the platelet surface by flow cytometry, assessed the total (and indirectly the internal) pool of GPIb by ELISA and measured the circulating amount of glycocalicin in plasma as a measure of proteolytic activity and platelet turnover. Von Willebrand factor was characterized by ELISA, by its ristocetin-cofactor activity and by multimer analysis. Botrocetin-induced agglutination was used for functional analysis. The data from 8 well-characterized cirrhosis patients indicate that total GPIb is insignificantly increased to 46,000 +/- 5,000 molecules/P (normal: 39,500 +/- 2,000 [SEM]), surface-GPIb is normal with some variability and that the glycocalicin levels are 2-3 times higher than would be expected from the platelet count (= 100 +/- 5 x 10(9)/l). Von Willebrand factor antigen levels and activity were 400-500% of normal with a 22% reduction of the high molecular weight multimers. A significant hyperagglutination response to botrocetin was observed with platelets from both patients and controls using patient plasma as a source of von Willebrand factor. In conclusion, a hyperresponsiveness rather than a defective platelet-von Willebrand factor interaction can be observed in cirrhosis which may compensate for other hemostatic problems and appears to be mediated primarily by increased levels of von Willebrand factor.
 ...
PMID:Quantitative and qualitative analysis of platelet GPIb and von Willebrand factor in liver cirrhosis. 749 66

Cirrhotic livers are considered to regenerate less actively than normal livers after hepatic resection. Little is known about the mechanisms responsible for impaired capacity of regeneration in cirrhotic liver. In the present study, we investigated the effect of phorbol ester on hepatocyte proliferation in healthy and cirrhotic hepatocytes, using one of the phorbol esters, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), which has a direct effect on activation of protein kinase C (PKC). Cirrhosis was established by the administration of carbon tetrachloride and phenobarbital to rats. Healthy and cirrhotic hepatocytes were isolated from Wistar male rats by a two-step collagenase perfusion technique. DNA synthesis was estimated by [3H]thymidine incorporation into DNA and by autoradiographic nuclear labeling index. [3H]Thymidine incorporation was measured 24 hr after hepatocytes were stimulated by appropriate reagents. TPA (50 nM) stimulated [3H]thymidine incorporation in healthy hepatocytes (control vs TPA, 991 +/- 247 vs 2569 +/- 766 mean +/- SEM cpm/microgram DNA; P < 0.05), whereas TPA (50 nM) failed to stimulate in cirrhotic hepatocytes (control vs TPA, 1144 +/- 184 vs 1304 +/- 187 cpm/microgram DNA; NS). Staurosporine, a specific PKC inhibitor, suppressed [3H]thymidine incorporation in TPA-stimulated healthy hepatocytes (806 +/- 263 cpm/microgram DNA; P < 0.05); however, it had no effect on cirrhotic hepatocytes (1295 +/- 180 cpm/microgram DNA; NS). An autoradiographic nuclear labeling index exhibited the same results with [3H]thymidine incorporation. We conclude that TPA stimulates hepatocyte proliferation in healthy rat hepatocytes but has no effect on cirrhotic hepatocytes.
 ...
PMID:Impaired phorbol ester-induced hepatocyte proliferation in cirrhosis. 772 25

Serial liver biopsy changes have been reviewed in 30 patients with Indian childhood cirrhosis (ICC) who were randomly allocated to receive treatment with penicillamine in a dose of 20 mg/kg/day, 10 of whom also received prednisolone, and five receiving placebo. The latter died within 185 (mean, 149) days of starting treatment. Nine receiving penicillamine died within 540 (mean, 338) days, but the remainder are well 5.1-9.3 years after commencing treatment. Initial biopsies showed severe hepatocellular injury, pericellular fibrosis, inflammatory infiltration, and orcein-staining granules. Second biopsies taken within 6 months of starting penicillamine usually showed persistence of inflammation and an increase in nodularity with thick and thin active septae. Subsequently the appearances were of an inactive micronodular cirrhosis, with reduction in septal inflammatory infiltrate, hepatocellular injury, and intensity of orcein staining. This further improved to a stage of incomplete fibrous septae. The last liver biopsies at 6-60 months (in 21 survivors) showed almost normal histology in four, incomplete fibrous septae in five, and inactive micronodular cirrhosis with thin septae in 12. Mean liver copper concentrations decreased from 1,407 (SEM, 121) micrograms/g at presentation to 925 (183), 317 (100), and 127 (35) at 6, 6-18, and > 18 months after starting treatment. By contrast, a second biopsy taken in the 6 months after diagnosis in placebo-treated children showed persistence of ICC with increase in inflammation, fibrosis, and orcein staining.
 ...
PMID:Reversal of Indian childhood cirrhosis by D-penicillamine therapy. 788 15

Arterial oxygen tension (Pao2), carbon dioxide tension (PaCO2), and vital capacity were measured preoperatively and one day postoperatively in patients with chronic hepatic cirrhosis having elective oesophageal injection sclerotherapy under general anaesthesia. The results were compared with the same measurements made in patients with chronic cirrhosis anaesthetised and scheduled to have injection sclerotherapy under general anaesthesia but who, because of variceal obliteration, only had an oesophagogastroscopy. In the injected group PaO2 decreased by 9.3 (3.0) mm Hg (1.2 (0.4) kPa) (mean (SEM)) (p < 0.02) but in the controls did not change. The difference between the two groups was significant (p < 0.02). Vital capacity decreased by 0.39 (0.08) litres (BTPS) (p < 0.01) after injection sclerotherapy but in the controls did not change. Again the difference between the two groups was significant (p < 0.02). In the injected group there was a significant correlation between the change in PaO2 and the percentage change in vital capacity (r = 0.787, p < 0.01) but no such relation was seen in control subjects. These results suggest that oesophageal injection sclerotherapy is associated with a restrictive defect in respiratory function one day after the injection caused, possibly, by sclerosant embolising to the lung.
 ...
PMID:Respiratory function after injection sclerotherapy of oesophageal varices. 795 5

Endotoxin sensitivity varies among animal species and appears to correlate with the presence of pulmonary intravascular macrophage (PIM). In rats, which lack PIM, we investigated the hypothesis that chronic cholestatic liver injury leads to induction of PIM and endotoxin sensitivity. Rats were randomized to either common bile duct ligation (BDL) or sham-surgery and studied at 1 wk (acute cholestasis), 2 wk (cholestasis, early cirrhosis), and 4 wk (cholestasis, established cirrhosis) after surgery. Intravascularly injected fluorescent latex microspheres (1 micron diameter) were taken up by large phagocytic cells in lung parenchyma of BDL rats (at 2 and 4 wk), while no uptake was observed in lungs from control rats. Electronmicroscopy revealed accumulation of large, mononuclear, macrophage-like cells containing ingested latex particles within the pulmonary capillaries. Pulmonary intravascular phagocytosis, as reflected in lung uptake of 99mTc microaggregated albumin (Microlite, mean particle diameter = 1 micron), averaged 0.7 +/- 0.1% (mean +/- SEM) of total injected dose in 13 control rats and progressively increased with time after BDL (1 wk, 1.7 +/- 0.2%; 2 wk, 10.0 +/- 3.0%; 4 wk 35.1 +/- 5.9%). Rats with biliary cirrhosis were markedly sensitive to the lethal effects of low dose endotoxin and demonstrated marked lung edema at the time of death. Furthermore, the lung uptake of intravascular 125I-lipopolysaccharide was increased five-fold in cirrhotic rats. We conclude that chronic biliary obstruction leads to the induction of pulmonary intravascular phagocytes and enhances endotoxin sensitivity in rats. Pulmonary intravascular phagocytosis in patients with advanced cirrhosis may account for their increased susceptibility to sepsis-induced adult respiratory distress syndrome.
 ...
PMID:Chronic biliary obstruction induces pulmonary intravascular phagocytosis and endotoxin sensitivity in rats. 796 47

Gastric mucosal bleeding time was measured prospectively in 25 patients with cirrhosis and portal hypertension undergoing routine sclerotherapy. Age and sex-matched controls without liver disease were also studied. Correlations were sought between gastric mucosal bleeding time and age, platelet count, prothrombin time, skin bleeding time, Child-Pugh score, variceal size before sclerotherapy, and degree of portal hypertensive gastropathy. Gastric bleeding time was prolonged in 12% of the patients with cirrhosis (mean, 3.24 minutes; SEM, 0.476) and in none of the controls (mean, 3.0; SEM, 0.171). No correlation was noted between gastric bleeding time and any of the above variables. The results of this study indicate that gastric mucosal bleeding time is prolonged in cirrhosis but is an independent physiologic parameter unrelated to any of the above-mentioned variables.
 ...
PMID:Gastric mucosal bleeding time in cirrhosis. 798 26

In ultrasonic imaging an adaptive two-dimensional filter (ATDF) can suppress randomly generated speckle using the ratio of the local variance to the local mean as the speckle recognition feature (R). The degree of smoothing depends on the difference between the recognition feature in the region to be filtered and the selected reference tissue. We have investigated the clinical application of ATDF for ultrasound B-mode images of liver abnormalities. Using the R values of normal liver as reference values, the ATDF images were displayed. Normal livers (n = 17, R = 2.19 +/- 0.14 M +/- SEM), fatty livers (N = 16, R = 1.89 +/- 0.15) and those with acute hepatitis (N = 10, R = 2.25 +/- 0.18) appeared smooth after application of the adaptive filter, but those diseases with higher R values, such as chronic hepatitis (N = 10, R = 3.04 +/- 0.30), cirrhosis (n = 16, R = 4.44 +/- 0.30), metastases (N = 16, R = 6.43 +/- 0.53) and hepatocellular carcinomas (N = 8, R = 7.92 +/- 0.85), were largely unsmoothed. In conclusion, ATDF allows differentiation of some forms of liver disease and may be helpful in the detection of microfocal echogenic textural lesions.
 ...
PMID:Tissue characterization using intelligent adaptive filter in the diagnosis of diffuse and focal liver disease. 799 73

Protein S is a vitamin K-dependent glycoprotein acting as a cofactor for activated protein C and thereby exerting an antithrombotic effect. When compared to values recorded in the 10 healthy normal weight normolipidemic control subjects (80.1% +/- 5.16; mean +/- SEM), plasma protein S-antigen (PS:Ag) level was found to be significantly (p < 0.01) decreased in the 11 patients with decompensated cirrhosis of the liver (54.72% +/- 4.89) and in the 12 surgical patients in critical condition (59.2 +/- 4.96), while obviously (p < 0.001) increased plasma levels were noted in the group including 20 overweight and hyperlipidemic subjects (113% +/- 3.1). Since the low PS:Ag level was associated with a decreased serum cholinesterase (CHE) activity, while both plasma PS:Ag and serum CHE activity were increased in overweight and hyperlipidemic subjects it is considered that impaired or respectively enhanced hepatic protein synthesis is at least partially responsible for changes affecting this antithrombotic plasma protein.
 ...
PMID:Plasma protein S-antigen (PS:Ag) in selected disease states. 808 8


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>